DESCRIPTION: (Adapted from the applicant's abstract and Specific Aims.) Obstructive sleep apnea syndrome (OSAS) results in transient periods of hypoxemia, hypercapnia and sleep interruption with associated acute and chronic sympathoexcitation and hypertension. Treatment of the disorder relieves many of the disorders and associated symptoms. The mechanism(s) explaining the acute and chronic states of sympathoexcitation have not been studied prospectively and may be relevant to the hypertension and elevated cardiovascular mortality in OSAS. Abnormalities of chemoreflex and baroreflex function have been speculated to explain the cardiovascular consequences of OSAS, but have not been studied prospectively.The Specific Aims are to: 1) determine the relative contribution of hypoxemia, hypercapnia, and effects of inspiratory effort to acute sympathoexcitation during sleep apnea or simulated apnea during wakefulness in patients with OSAS and healthy subjects; 2) develop a model of these reflex-mediated effects including interactive effects between hypoxemia and hypercapnia in patients with OSAS and healthy subjects; 3) determine the effect of sleep interruption on baseline conditions, chemoreflex and baroreflex function in normotensive and hypertensive patients with OSAS and in control subjects; 4) determine the effect of short-term or long-term treatment of OSAS with nasal CPAP on chronic sympathoexcitation, chemoreflex sensitivity and baroreflex sensitivity during wakefulness; and 5) determine the relation of chronic sympathoexcitation, chemoreflex sensitivity and baroreflex sensitivity during wakefulness to the presence of clinical hypertension in patients with OSAS. Understanding the control of sympathetic nerve activity (SNA) in these patients may lead to improved management of this condition and may lend provide new insight into the importance of chemoreflex control of SNA in healthy and diseased humans.